MindMap Gallery urinary tract disease
Pathology summarizes and organizes knowledge points to help learners understand and remember. Straight to the point, it can be used as study notes and review materials to help you systematically review and consolidate the knowledge you have learned. The knowledge points are systematic and comprehensive. I hope it will be helpful to everyone! Suitable for exam review.
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urinary tract disease
Anatomy and pathogenesis
filter membrane
Capillary endothelial cells (innermost layer)
70-100nm window, sialoglycoprotein (positively charged)
Anions are deposited here
Basement membraneGBM
mechanical barrier
vulnerable to immune attack
Anti-GBM antibody exhibits continuous linear fluorescence
Podocytes (visceral epithelial cells)
Foot processes constitute the most important charge barrier (negative charge)
Allows small molecules to pass through but proteins cannot
Cations are deposited here
Mesangial area (connecting each filtration membrane)
mesangial cells
Secrete inflammatory mediators
Phagocytosis
Neutral complexes are deposited here
parietal epithelial cells
outermost layer of glomerulus
Pathogenesis (antigen-antibody reaction)
exogenous
Bacteria, drugs, various serums (circulating immune complexes)
endogenous
Glomerular antigen (for filtration membrane) (in situ immune complex)
non-glomerular antigen
Immunofluorescent substances
complement antibody
Glomerulonephritis (proliferative)
some clinical syndromes
acute nephritic syndrome
Hematuria, edema (sodium and water retention), and high blood pressure
acute diffuse proliferative glomerulonephritis
rapidly progressive nephritic syndrome
ARF
Rapidly progressive glomerulonephritis (crescentic)
Nephrotic syndrome (most common)
Membranous glomerulopathy (adults)
Minimal change glomerulopathy (children)
Massive proteinuria (>3.5g/L) and hypoalbuminemia
Asymptomatic hematuria or proteinuria
Recurrent or persistent episodes of hematuria
IgA nephropathy
chronic nephritic syndrome
Polyuria, nocturia, etc.
chronic glomerulonephritis
acute diffuse proliferative glomerulonephritis
Nickname
Intracapillary proliferative glomerulonephritis
Cause
Group A streptococcal infection leads to circulating IC deposition
Pathological changes
naked eye
Big red kidneys (congestion), flea-bitten kidneys (bleeding spots)
light microscope
Glomerular endothelial cell and mesangial cell proliferation
Neutrophil infiltration
Glomerular capillary fibrinoid necrosis (severe)
electron microscope
Hump-shaped high electron density deposition between podocytes and basement membrane
clinical manifestations
hematuria
acute nephritic syndrome
Anti-O antibody positive
Rapidly progressive glomerulonephritis
Nickname
crescentic glomerulonephritis
Rapidly progressive glomerulonephritis
Types
Type 1
anti-GBM antibodies
Type 2
IC deposition
Pathological changes
light microscope
Glomerular crescents (parietal epithelial cell proliferation, extravasated mononuclear cells)
electron microscope
GBM defect fracture
Immunofluorescence
Type 1
linear fluorescence
Type 2
granular fluorescence
Type 3
No fluorescence
clinical manifestations
Rapidly progressive nephritic syndrome (kidney failure)
Goodpasture syndrome
Pulmonary hemoptysis (immune cross-attack)
prognosis
Difference
kidney disease
membranous nephropathy
People prone to hair loss
aldult
Pathological changes
naked eye
Great White Kidney
light microscope
Early glomeruli are normal
Advanced diffuse basement membrane thickening
PASM stained basement membrane tooth comb
electron microscope
The foot processes disappear and there are large amounts of electron-dense deposits between the basement membrane and the epithelium.
basilar membrane spikes
Immunofluorescence
Granular fluorescence (immunoglobulin complement)
minimal change glomerulopathy
People prone to hair loss
child
Cause
epithelial cell damage
Filter membrane anion loss
No IC participation
Pathological changes
naked eye
Yellow-white streaks (lipid nephropathy)
light microscope
Normal glomerular structure
Fatty change and hyaline degeneration in the proximal tubule epithelium
electron microscope
Diffuse podocyte foot process effacement
Immunofluorescence
Negative
Clinical features
highly selective proteinuria
prognosis
Yes, corticosteroid treatment is 90% effective
membranoproliferative glomerulonephritis
Nickname
Mesangial capillary glomerulonephritis
Cause
Type 1
IC activates complement
Type 2
C3 nephritis factor activates the accessory pathway, resulting in hypocomplementemia
Pathological changes
light microscope
Mesangial and stromal proliferation inserts subcapillary endothelium
Endothelial cell proliferation may occur
Resulting in double lines or double tracks (two layers of endothelial cells)
electron microscope
Type 1
Electron-dense deposits under endothelial cells
Type 2
high density of deposits in the basement membrane
Immunofluorescence
Type 1
Deposition of C3 and C1q etc.
Type 2
C3 deposition
Mesangial proliferative glomerulonephritis
light microscope
Diffuse mesangial and stromal cell proliferation
electron microscope
Electron-dense deposits in the mesangium
IgA nephropathy
clinical manifestations
recurring episodes of hematuria
light microscope
Increased mesangial cells and basement membrane matrix (most typical)
focal segmental hyperplasia
Crescents can be formed
electron microscope
Electron-dense deposition in the mesangium
Immunofluorescence
IgA deposition in mesangial area
chronic glomerulonephritis
Cause
Various types of glomerulonephritis develop from
naked eye
secondary granular pyknotic kidney
light microscope
Glomerular hyalinization and sclerosis
Renal tubular-interstitial nephritis
acute pyelonephritis
Cause
E. coli ascending infection (most common)
golden grape descending infection
Nature of the lesion
Acute suppurative inflammation (exudative inflammation)
Pathological changes
naked eye
Abscess formation on the cut surface
Renal pelvic mucosa is congested and edematous, with purulent exudation on the surface
under the mirror
Interstitial suppurative inflammation or abscess formation
Neutrophil accumulation and tubular necrosis in the renal tubular lumen
chronic pyelonephritis
Cause
Urinary tract obstruction
Bladder and ureteral reflux
intrarenal reflux
Nature of the lesion
chronic suppurative inflammation
Pathological changes
interstitial plasma cell lymphocyte infiltration
Glomerular and interstitial fibrosis (hyalinization)
Colloidal casts in the renal tubules
focal lesion
kidney and bladder tumors
renal cell carcinoma
origin
Renal tubular epithelial cells (adenocarcinoma)
naked eye
Most common in the upper pole of kidney
pseudocapsule
Colorful cross-section
under the mirror
Clear cell type (mainly)
Tumor cells have abundant and transparent cytoplasm
The interstitium is rich in capillaries and sinusoids
papillary carcinoma
Grows very fast
clinical manifestations
Hematuria, lumps, pain
Urinary tract and bladder epithelial tumors
Predisposed areas
trigone of bladder
origin
transitional epithelium
Grading
low-grade papillary urothelial carcinoma
low-grade papillary urothelial carcinoma
High-grade papillary urothelial carcinoma (invasive type)
clinical manifestations
painless hematuria
Nephroblastoma (Wilims tumor)
origin
metanephric embryonic tissue
People prone to hair loss
child
in general
A single large solid mass
fish-like cut surface